Degerman Sofie, Josefsson Maria, Nordin Adolfsson Annelie, Wennstedt Sigrid, Landfors Mattias, Haider Zahra, Pudas Sara, Hultdin Magnus, Nyberg Lars, Adolfsson Rolf
Department of Medical Biosciences, Umeå University, Umeå, Sweden.
Centre for Demographic and Ageing Research, Umeå University, Umeå, Sweden.
Neurobiol Aging. 2017 Jul;55:167-171. doi: 10.1016/j.neurobiolaging.2017.02.009. Epub 2017 Feb 20.
Epigenetic alterations during aging have been proposed to contribute to decline in physical and cognitive functions, and accelerated epigenetic aging has been associated with disease and all-cause mortality later in life. In this study, we estimated epigenetic age dynamics in groups with different memory trajectories (maintained high performance, average decline, and accelerated decline) over a 15-year period. Epigenetic (DNA-methylation [DNAm]) age was assessed, and delta age (DNAm age - chronological age) was calculated in blood samples at baseline (age: 55-65 years) and 15 years later in 52 age- and gender-matched individuals from the Betula study in Sweden. A lower delta DNAm age was observed for those with maintained memory functions compared with those with average (p = 0.035) or accelerated decline (p = 0.037). Moreover, separate analyses revealed that DNAm age at follow-up, but not chronologic age, was a significant predictor of dementia (p = 0.019). Our findings suggest that young epigenetic age contributes to maintained memory in aging.
衰老过程中的表观遗传改变被认为是导致身体和认知功能下降的原因，而加速的表观遗传衰老与疾病及晚年的全因死亡率相关。在本研究中，我们评估了不同记忆轨迹组（保持高性能、平均下降和加速下降）在15年期间的表观遗传年龄动态变化。对来自瑞典桦树研究的52名年龄和性别匹配个体的血液样本进行了表观遗传（DNA甲基化[DNAm]）年龄评估，并计算了基线时（年龄：55 - 65岁）和15年后的年龄差（DNAm年龄 - 实际年龄）。与记忆功能平均下降（p = 0.035）或加速下降（p = 0.037）的个体相比，记忆功能保持的个体的DNAm年龄差更低。此外，单独分析显示，随访时的DNAm年龄而非实际年龄是痴呆的显著预测因素（p = 0.019）。我们的研究结果表明，年轻的表观遗传年龄有助于在衰老过程中保持记忆。
